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Women prefer ‘manly’ men when poor health is their country’s norm

March 17, 2010 By vani Leave a Comment

London, March 17 (ANI): Women who live in countries where poor health is the norm prefer more masculine-looking men, a new research has found.

On the hand, women who live in healthier countries prefer more feminine-looking men, according to the study.

Psychologists say their research suggests that masculine men have the greatest appeal for women who live in areas where a strong genetic make-up is critical for survival.

“When women are choosing a mate, they”re weighing up two different things. On the one hand a really attractive, high genetic quality mate will give them very healthy offspring. On the other, there is getting “investment” from a mate – one who”ll be a good dad,” The Guardian quoted Lisa DeBruine, who led the study at Aberdeen University in the UK, as saying.

“Men who are really attractive tend to be able to pursue whatever mating strategy is best for them. They are more likely to prefer short-term relationships. More feminine men tend to be better providers,” she added.

The study of women in 30 countries showed that women were more likely to choose a masculine-looking partner if their country scored low on a health index based on World Health Organisation mortality figures.

On contrary, in countries where people have a longer lifespan, women favoured more feminine-looking men, even though they might not have the healthiest genes available.

DeBruine said: “Certain environmental factors shift the balance when a woman is choosing a mate, and health is one of those. If a woman lives in an environment where there are lots of pathogens and disease, they are more likely to trade off a good investment in favour of better health for their children. In places where health is less of an issue, women are not so willing to do that.”

The study has been published in Proceedings of the Royal Society B. (ANI)

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Vitamin D vital for activating our immune defenses

March 8, 2010 By vani Leave a Comment

London, March 8 (ANI): Vitamin D plays an important role in activating our immune defenses against infectious diseases like flu, says a new study.

According to the research, without sufficient intake of the vitamin, the killer cells of the immune system – T cells – will not be able to react to and fight off serious infections in the body.

For T cells to detect and kill foreign pathogens such as clumps of bacteria or viruses, the cells must first be ”triggered” into action and ”transform” from inactive and harmless immune cells into killer cells that are primed to seek out and destroy all traces of a foreign pathogen.

Scientists at the University of Copenhagen discovered that the T cells rely on vitamin D in order to activate and they would remain dormant, ”naive” to the possibility of threat if vitamin D is lacking in the blood.

For the research team, identifying the role of vitamin D in the activation of T cells has been a major breakthrough.

“Scientists have known for a long time that vitamin D is important for calcium absorption and the vitamin has also been implicated in diseases such as cancer and multiple sclerosis, but what we didn”t realize is how crucial vitamin D is for actually activating the immune system – which we know now,” the authors said.

The study has been published in the latest edition of Nature Immunology. (ANI)

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HIV uses several routes to escape immune system pressure

September 19, 2009 By admin Leave a Comment

Washington, September 19 (ANI): Researchers at the Emory Vaccine Center have shown that HIV relies upon a number of strategies rather than use any preferred escape route to escape immune system pressure.

The human immune system has the ability to temporarily overpower HIV in early infection.

Studies conducted in the recent past have shown that most newly infected patients develop neutralizing antibodies. These are blood proteins that glob onto the virus and would allow patients to defend themselves – if they were facing only one target.

However, the problem occurs when HIV mutates, and disguises itself enough to get away from the antibodies. The virus eventually wears down the immune system into exhaustion.

The Emory team’s findings attain significance as they suggest that even if any scientist succeeds in identifying a vaccine component that can stimulate neutralizing antibodies, HIV’s capacity for rapid mutation could still be a confounding factor.

Dr. Cynthia Derdeyn, associate professor of pathology at Emory University School of Medicine, Emory Vaccine Center and Yerkes National Primate Research Center, says that a single type of neutralizing antibody may not be enough to contain HIV.

“These neutralizing antibodies work really well – they hit the virus fast and hard. But so far, every time we look, the virus escapes,” she says.

During the study, the researchers took blood samples from the participants a few weeks after infection occurred, and then later as two participants’ immune responses continued.

They isolated individual viruses over the first two years of HIV infection, and tested how well the patients’ own antibodies could neutralize them.

“In one patient where we had very early samples, there was evidence that neutralizing antibody came up within weeks, and that’s earlier than what was previously thought,” Derdeyn says.

In both patients, some viruses mutated part of their outer proteins so that after the mutation, an enzyme would be likely to attach a sugar molecule to it.

Though the sugar molecule interferes with antibody attack, this tactic, known as the “glycan shield”, was not observed in all cases.

Other viruses mutated the part of the outer protein that the neutralizing antibodies stick to directly. In both patients, many changes in the virus’ genetic code were necessary for escape.

“We need to understand early events in the immune response if we are going to figure out what a potential vaccine should have in it. What we can show is that even in one patient, several escape strategies are going on,” Derdeyn says.

According to her, that means that in order to be immune to HIV infection, someone may need to have several types of neutralizing antibodies ready to go.

Seeing how the virus mutates will allow researchers to choose the best parts to put in a vaccine, she says.

The results are online and scheduled for publication in the September issue of the journal Public Library of Science Pathogens.(ANI)

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Vaccine for urinary tract infections comes closer to reality

September 19, 2009 By admin Leave a Comment

Washington, Sept 18 (ANI): A simple vaccine may soon be available to protect against urinary tract infections, thanks to researchers from University of Michigan.

The study conducted over mice showed that the vaccine prevented infection and produced key types of immunity.

It alerts the immune system to iron receptors on the surface of Escherichia coli bacteria that perform a critical function allowing infection to spread.

Administered in the nose, it induces an immune response in the body’s mucosa, a first line of defense against invading pathogens. The response, also produced in mucosal tissue in the urinary tract, should help the body fight infection where it starts.

The researchers used novel systematic approach, combining bioinformatics, genomics and proteomics, to look for key parts of the bacterium that could be used in a vaccine to elicit an effective immune response.

The team, led by Dr. Harry L.T. Mobley, screened 5,379 possible bacterial proteins and identified three strong candidates to use in a vaccine to prime the body to fight E. coli.

Mobley’s team is currently testing more strains of E. coli obtained from women treated at U-M.

If the robust immunity achieved in mice can be reproduced in humans, it could be the first ever vaccine for urinary tract infections.

Most of the strains produce the same iron-related proteins that can be vaccine targets, an encouraging sign that the vaccine could work against many urinary tract infections.

The findings are published in the open-access journal PLoS Pathogens. (ANI)

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Parasites’ quirky trick to persuade immune cells to invite them in for dinner

August 21, 2009 By admin Leave a Comment

Washington, Aug 21 (ANI): Scientists from Imperial College London have found that parasite leishmania tricks immune system to let it enter the body and cause skin infection.

Leishmaniasis is an infection caused by Leishmania parasites that cause disfiguring and painful skin ulcers, and in severe cases the infection can also spread to the internal organs.

Patients with the infection often suffer from social exclusion because of their disfigurement.

Leishmania parasites are transmitted by sand flies. After the parasites infect a sand fly, they make a sticky gel so that when the fly bites a human, it regurgitates this gel into the body.

The new study conducted over mice showed that the gel persuades immune cells known as macrophages to feed the parasites, rather than killing them.

The gel helps the parasites to establish an infection by enticing macrophages to the bite site. Macrophages usually kill invading pathogens by eating and digesting them.

However, the gel persuades macrophages to engulf the parasites and feed them rather than digest them.

This happens within the first few days following infection, enabling the parasites to establish themselves and infect the skin.

“Leishmaniasis is a very debilitating disease, yet we know comparatively little about the way the parasites are transmitted by sand flies,” said Dr Matthew Rogers, lead author of the study from the Division of Investigative Science at Imperial College London.

“This is because when scientists study the disease they usually inject the parasite into tissues without including the gel or the sand fly’s saliva. Our new research shows that we must consider the way the parasites enter the body – along with the gel and saliva – if we are to recreate infection and get an accurate picture of what is going on.

“Our new research shows that Leishmania parasites are very cunning – they make their own gel to control the human immune system so they can establish a skin infection.

“There is more work to be done here – our previous work in mice has suggested that injecting a synthetic version of the gel into people might provide them with some protection against infection and we would like to explore this further,” he added.

The study is published in PLoS Pathogens. (ANI)

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Waste by-product of malaria parasite’s reproductive process linked to devastating fever

August 21, 2009 By admin Leave a Comment

Washington, August 21 (ANI): Studying hemozoin – a crystal-like by-product released during reproduction among parasites from the Plasmodium family – may help understand why malaria leads to devastating inflammation and fever, according to a Canadian study.

Lead researcher Dr. Martin Olivier, of McGill University in Montreal, points out that, inside the human body, the malaria parasite infects red blood cells where it survives and reproduces by feeding on the cells’ contents.

Eventually, says the researcher, the cells burst and release the parasites and hemozoin.

“Our results describe the mechanism by which the hemozoin activates the immune system, resulting in the production of inflammation mediators and in the high fever that we witness in malaria patients,” said study’s first-author Dr. Marina Tiemi Shio, of the Research Institute of the McGill University Health Centre (RI-MUHC).

According to the researchers, hemozoin is first ingested by “cleaning” cells called macrophages, which leads to a chain reaction ending in the activation of the inflammasome: an important structure inside immune cells which lead to inflammation.

They say that the activation of the inflammasome leads to the production of the body’s fever mediator, interleukin beta (IL-beta).

“Our work is a milestone in that it is the first study that reveals the enzymes that act as intermediary between the hemozoin and inflammasome. Now our picture of the process that goes from infection to fever is more or less complete,” said Dr. Olivier.

“On the other hand, we also proved that malaria is too complex to be narrowed down to one single mechanism. In the absence of either IL-beta or a functional inflammsaome, the development of the disease is delayed but not completely stopped. Although the discovery of this relationship is important, there are other mechanisms at work,” he added.

Even though scientists have been familiar with the mechanisms that go from the activation of the inflammasome to the onset of the malaria symptoms, none of the previous studies has ever shown the beginning of the process.

“These results prove the primary role hemozoin plays in the development of malaria, and designates it as a favoured choice for future innovative treatments,” said Dr. Olivier.

The researchers believe it will be possible to familiarize the immune system to small quantities of hemozoin, and diminish the inflammatory response in the event of infection, according to a principle similar to that of vaccines.

The results of the study have been published in the journal PLoS Pathogens. (ANI)

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HIV-1 destroys immune response in the gut within days of infection

July 7, 2009 By admin 1 Comment

Washington, July 7 (ANI): Researchers have found that HIV-1 virus moves rapidly in the body, and damages the B-cell antibody-producing system in the gut, within days of infection.

The study by Centre for HIV/AIDS Vaccine Immunology is the first to examine what happens to B cells in the gut in the earliest stage of HIV-1 infection.

“These new data show that damage to the antibody arm of the immune system begins quickly, within days. We know that by 80 days, half of the generative microenvironments for antibodies within the immune system in the gut are destroyed,” said Dr. Barton Haynes, senior author of the study.

The findings could solve one of the big mysteries in HIV-why the B cell, or antibody response, is so slow to arise in the first place and turns out to be so weak after it does, that it is unable to offer any kind of meaningful defence.

B cells that make antibodies against invading microbes are born in the bone marrow, but migrate out and mature in different locations throughout the body.

Some wind up in the intestine and settle in stretches of lymph node-like follicles called Payer’s patches, which are found at the bottom of the small intestine, where they wait to rise up against incoming bacteria, viruses, or other pathogens.

“Unfortunately, we found they are no match for HIV-1,” said Anthony Moody, a lead author of the study.

For the study, the researchers examined B cells in blood as early as 17 days after viral transmission, and in lymph tissue in the gut beginning at 47 days after transmission in 40 people infected with HIV-1.

They compared their findings with similar tissue from healthy controls, and found that even at the early stage, HIV-1 had already ravaged the gut’s B cell arm of the immune system.

The vast majority of the follicles in the Payer’s patches had been damaged.

“HIV-1 turns on the immune system, but turns it on in the wrong way. We found that it was churning out all sorts of B cells. Some appeared to be reactive against HIV-1, but others appeared reactive to things like influenza as well as self molecules,” said Moody.

Besides, it was found that by as early as 17 days after transmission, HIV-1 decreased the numbers of naive B cells – cells that may have had the potential to mature into potent infection-fighters.

The researchers are hoping that the findings may lead to a successful AIDS vaccine.

The study has been published in the open access journal PLoS Medicine. (ANI)

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Cleaning agent may help in superbug battle

June 27, 2009 By admin Leave a Comment

London, June 27 (ANI): A cleaning agent, developed to stop mould growth in bakeries and fish factories, has been found effective in killing hospital superbugs, say researchers.

The research team from Manchester Royal Infirmary (MRI) have found that agent Byotrol has cut levels of MRSA on wards by one third.

Byotrol, an antimicrobial technology developed by a Manchester-based paint firm, has a polymer-based structure, which enables it to kill bacteria, like MSRA, days after being first applied.

The polymer is said to create a surface tension effect, which operates like a flytrap that literally tears apart the bacteria when they come into contact.

“These are very impressive results. Our study has shown a reduction of one third in levels of MRSA in the ward when the new disinfectant was compared with the gold-standard NHS bleach-based cleaning agent,” the Telegraph quoted Dr Andy Dodgson, consultant microbiologist at the MRI who led the trial as saying.

“The new disinfectant has a clear role to play in helping hospitals in the battle to control HCASIs. Cutting the level of pathogens on the wards rescues the risk to patients of picking up an infection.

“The demonstration of a residual antibacterial effect is a major new discovery which will be an additional weapon for the NHS in the fight against superbugs,” he added.

Stephen Falder, the scientist who invented Byotrol, said: “I suppose you could say this is a prevention for superbugs that almost never happened. I began developing it as a protection to stop mould on paints. It grew from there.”

The study will be published in British Journal of Infection Control. (ANI)

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How bacteria’s in-built thermometer helps spread infection

May 21, 2009 By admin Leave a Comment

Washington, May 21 (ANI): Scientists at the Helmholtz Centre for Infection Research (HZI) have for the first time shown how bacteria measure temperature, and thereby cause intestinal infection.

The HZI researchers at Braunschweig and the Braunschweig Technical University have found that bacteria of the Yersinia genus have a unique protein thermometer – the protein RovA – that helps them in the infection process. ovA is a multi-functional sensor that measures both the temperature of its host and the host’s metabolic activity and nutrients.

If these are suitable for the survival of the bacteria, the RovA protein activates genes for the infection process to begin.

Yersinia is known for triggering various different diseases, one of the well-known diseases is the Yersinia pestis type which caused the Plague in medieval times, leading to the death of around a third of Europe’s population.

The Yersinia enterocolitica and Yersinia pseudotuberculosis species cause an inflammation of the intestines following food poisoning.

The Yersinia bacteria contain invasin as a surface protein to help them penetrate the intestinal cells, leading to heavy bouts of diarrhoea.

Led by Petra Dersch, the researchers have now identified how the RovA protein plays a key role in the various stages of Yersinia infection.

The protein reads the temperature for the bacteria, on the basis of which it either contains the factors required for the infection to begin or else adapts to life within the host.

“The functioning of RovA in this way is unique among bacteria,” said Dersch.

If inhabiting an environment of around 25 degree Celsius, the protein RovA ensures that the Yersinia bacteria form invasin as a surface protein, which ensures that the bacteria can penetrate the intestinal cells immediately upon reaching the 37 degree Celsius intestine via food.

The warm environment enables RovA to alter its form and de-activates the gene for invasin production.

Without invasin on their surface, the Yersinia bacteria are invisible to the body’s immune system, thus making it possible for RovA to now activate other genes in the bacteria to adapt the Yersinia metabolism with that of the host.

“We have long been searching for the mechanisms which regulate RovA activity. It was therefore all the more surprising to discover that RovA controls various processes by acting as a thermometer and as such is self-regulating,” said Dersch.

The results have been published in the current online edition of the PLoS Pathogens science magazine. (ANI)

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HIV’s ‘hide and seek’ could make it weaker

May 9, 2009 By admin Leave a Comment

Melbourne, May 9 (ANI): HIV usually plays a game of hide and seek to dodge the immune system, but a new study has claimed that such playfulness actually makes the deadly virus vulnerable at times, according to an Australian study.

The finding could offer insights into the treatment of HIV during the early stages of infection.

At the time of entering a new host, HIV includes a form that researchers call escape mutant.

Although the escape mutant virus is better at evading our immune system, it is weaker and replicates slower than the wild-type form.

“When HIV infects a new host it needs to adapt to this new environment,” ABC News quoted lead author and PhD student Liyen Loh, of the Department of Immunology and Microbiology at The University of Melbourne, as saying.

She added: “The mutations often revert to the original wild-type virus, allowing the virus to regain a fitter state, or the changes may be retained, depending on the individual’s immune system. This explains why some individuals have better clinical outcomes than others.”

In the study, the researchers from the University of Melbourne and the University of Sydney analysed the evolution of the virus using macaque monkeys by infecting them with different quantities of wild-type SIV (the non-human equivalent of HIV) and escape mutant SIV.

They then measured the growth of the virus for the next three months to find out how much time the escape mutant form took to revert back to its fitter wild-type state.

“In the absence of immune pressure the virus will not stay in its weakened state, because it is not beneficial for the virus,” said Loh.

It was discovered that in animals infected with the escape mutant virus, it took 8 days for wild type to appear and it took 8 weeks for them to outnumber the escape mutant form.

The researchers also found that the genetic makeup of the virus affected how fast the virus adapts in the host.

“If (the macaques) get infected with purely one strain of virus it will take longer to adapt to the new host,” said Loh.

In her opinion, the study only focused on one structural part of the virus that mutates, and also claimed that there are many “other bits” that affect how the HIV evolves in an infected individual.

The study has been published in the PLoS journal Pathogens. (ANI)

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How ants identify dead nestmates

May 6, 2009 By admin Leave a Comment

Washington, May 6 (ANI): A dead ant is usually identified by its nestmates and removed from the colony, thus limiting the risk of colony infection by pathogens from the corpse. But how the news of a resident’s death is communicated among the nestmates has not been clearly known to date.

For a long time, entomologists have thought that dead ants release chemicals created by decomposition (such as fatty acids) that signal their death to the colony’s living ants.

But, now, UC Riverside entomologists working on Argentine ants provide evidence for a different mechanism for how necrophoresis – the removal of dead nestmates from colonies – works.

They have said that all ants, both living and dead, have the “death chemicals” continually, but living ants have them along with other chemicals associated with life – the “life chemicals.”

When an ant dies, its life chemicals dissipate or are degraded, and only the death chemicals remain.

“It’s because the dead ant no longer smells like a living ant that it gets carried to the graveyard, not because its body releases new, unique chemicals after death,” said Dong-Hwan Choe, the lead author of the research paper.

“There is no mistaking that it is the dissipation of chemical signals associated with life rather than the increase of a decomposition product ‘death cue’ that triggers necrophoric behaviour by Argentine ants,” he said.

The researchers used analytical chemistry techniques to identify the “signals of life” in the Argentine ant: the chemicals dolichodial and iridomyrmecin.

“These chemicals, or compounds similar to them, are found in numerous ant species that display necrophoresis. Therefore, these ant species also are likely to have necrophoric behavior triggered by the decrease or absence of chemical signs of life, rather than by cues associated with death. We plan to research this next,” said Choe.

He added that dolichodal, iridomyrmecin, or similar compounds are found also in other insects, such as thrips, stick insects, aphids and rove beetles.

“Understanding the exact mechanism of ant necrophoresis will help researchers develop a more environmentally friendly pest management strategy by which we can achieve results with smaller amounts of insecticide,” Choe said.

The study has been published online in the early edition of the Proceedings of the National Academy of Sciences. (ANI)

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Groundbreaking First Response Spray Now Available in Europe

April 17, 2009 By admin Leave a Comment

Solution Provides 99.99 Percent Reduction of Many Dangerous Pathogens

UNION, Ky., April 15 /PRNewswire/ — Union Springs Pharmaceuticals, LLC today
announces the European distribution of its flagship product, MyClyns, a
portable spray that reduces 99.99 percent of many harmful pathogens and helps
prevent infection. European first responders and public safety officials will
now have access to the spray, which is a critical component to effective,
portable protection.

(Photo: http://www.newscom.com/cgi-bin/prnh/20090415/CL99689 )

MyClyns is available from a number of distributors throughout Europe.

After coming into contact with bodily fluids from a potentially infected
person, first responders can quickly and easily spray MyClyns in their eyes,
mouth or on other points of contact. Response time is critical to lower the
chances of becoming infected after an exposure, and MyClyns offers immediate
protection.

The pocket-sized units contain a powerful solution that has been found to
reduce 99.99 percent of HIV-1, Hepatitis C, MRSA, TB, and 60 pathogens in
independent laboratory testing. The spray is alcohol-free and proven safe for
use on all mucous membranes, including the eyes, ears, nose, and mouth.

“MyClyns has found significant success within the public safety sector, as
first responders are frequently exposed to the dangers of bodily fluids and
other harmful pathogens,” says Union Springs Pharmaceuticals president Joel
Ivers. “The expansion of this product into European markets is in response to
the need for personal protection anywhere in the world where public safety
officials risk dangerous exposure.”

The spray has already proven to be an asset to public safety officials,
military, corrections, and EMS in the United States and Canada.

New Orleans EMS Deputy Director Carl Flores agrees. “One of our employees had
a combative patient who was HIV positive spit in his face,” said Flores. “He
used MyClyns and felt better knowing it was readily available for this
incident. As a manager, I cannot tell you how pleased I am to provide our
employees with this added layer of protection and sense of confidence when
they needed it most.”

Visit www.myclyns.eu for more information about the product.

About Union Springs Pharmaceuticals, LLC
Union Springs Pharmaceuticals, LLC specializes in providing innovative
infection control products for the EMS, fire, law enforcement, corrections,
military, government, healthcare, and consumer markets. Union Springs
Pharmaceuticals offers personal and environmental exposure response products
including MyClyns, the revolutionary personal protection spray that can be
applied into the eyes, nose, and mouth. Union Springs also offers the T-5000
and T-5000V P95 respirators, the only disposable respirators with
antibacterial and antiviral technology. More information on Union Springs
Pharmaceuticals and its products can be found at www.uspharma.com.

SOURCE Union Springs Pharmaceuticals, LLC

Bryan Reynolds, Union Springs Pharmaceuticals, LLC, +1-859-384-4029,
breynolds@uspharma.com

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Attacking parasite may help deal with honeybee colony collapse

April 15, 2009 By admin Leave a Comment

Washington, Apr 16 (ANI): By isolating the parasite behind honeybee colony depopulation syndrome, also known as colony collapse disorder in the USA, scientists have found a possible cure for the infection.

Spanish researchers isolated the parasite Nosema ceranae (Microsporidia) from professional apiaries suffering from honeybee colony depopulation syndrome, and found that it could be the only cause of the disease.

The researchers treated the infected surviving under-populated colonies with the antibiotic drug, flumagillin, and showed complete recovery of all infected colonies.

Honeybees are attacked by numerous pathogens, including viruses, bacteria, fungi, and parasites.

However, the molecular pathogenesis for most of these diseases is poorly understood, which in turn hampers the development of new ways to prevent and combat honeybee diseases.

However, this is the first time that this bug been identified as the primary cause in professional apiaries.

“Now that we know one strain of parasite that could be responsible, we can look for signs of infection and treat any infected colonies before the infection spreads,” said Dr Higes, principle researcher.

The finding could help prevent the continual decline in honeybee population, which has recently been seen in Europe and the USA.

The study has been published in the new journal from the Society for Applied Microbiology: Environmental Microbiology Reports. (ANI)

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Vitamin D supplementation may worsen autoimmune disease

April 9, 2009 By admin Leave a Comment

Washington, April 9 (ANI): Low levels of vitamin D in patients with autoimmune disease may be a result rather than a cause of the disease, and supplementing with this nutrient may worsen a patient’s condition, according to a review.

Researchers at the California-based non-profit Autoimmunity Research Foundation, who have authored the review, say that vitamin D may provide short-term relief by lowering inflammation, but it may exacerbate disease symptoms over the long-term.

Written under the guidance of professor Trevor Marshall of Murdoch University, Western Australia, the paper mainly focuses on the actions of a form of vitamin D derived from food and supplements, known as 25-hydroxyvitamin D (25-D).

The researchers say that 25-D inactivates rather than activates its native receptor, the Vitamin D nuclear receptor (VDR), and subsequently the immune response.

They say that this, though lowers the inflammation caused by bacteria, allows them to spread more easily in the long-run.

According to them, low levels of 25-D are frequently noted in patients with autoimmune disease because they are naturally down-regulated in response to VDR dysregulation by chronic pathogens.

Under such circumstances, supplementation with extra vitamin D may not only be counterproductive but harmful also, because it slows the ability of the immune system to deal with such bacteria.

“Vitamin D is currently being recommended at historically unprecedented doses. Yet at the same time, the rate of nearly every autoimmune disease continues to escalate,” points out Amy Proal, one of the paper’s co-authors

A research article on this study has been published in Autoimmunity Reviews. (ANI)

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Sex workers prefer indirect screening for sexually transmitted diseases

April 2, 2009 By admin Leave a Comment

Washington, Apr 1 (ANI): When it comes to screening for sexually transmitted infections (STIs), female commercial sex workers (CSW) prefer self-collection of samples to traditional tests, revealed researchers at the University of Westminster.

The simple and convenient screening method used by the researchers didn’t require the sex workers to attend clinics.

The women were given tampons that they could use to collect their own samples, and post them to a laboratory.

The results also indicated that the women in the study found self-collection of samples very easy and the testing methods used in the study proved to be more accurate than traditional tests.

Lead author of the study, Dr Patrick Kimmitt, pointed out that despite their risk of exposure to STIs, female CSW were reluctant to attend clinics for regular screening for such infections.

That might due to unsuitability of opening times, fear of stigma or the false concern of the possibility of being reported to the police.

“Point of care testing” delivered at their workplace is more attractive to this patient group.

The study involved 65 CSW, all of whom were asked to complete a questionnaire in which they indicated their preferences for screening and ease of use of sample collection.

The samples were processed in the laboratory using a method called PCR (Polymerase Chain Reaction) which rapidly detects a unique DNA sequence in three of the micro-organisms that cause STIs – gonorrhoea, Chlamydia and Trichomonas.

The researchers also collected samples and screened for those pathogens using traditional laboratory methods for comparison.
The results showed that all the women found self-collection of samples very easy, and preferred this method of screening for STIs.

Furthermore, more cases of gonorrhoea and Chlamydia were found using the PCR method compared to traditional methods.

“If this is seen to be an acceptable method then it could be considered as a possible testing device for other patient groups who also find it difficult, or are reluctant, to access mainstream sexual health screening services, such as women in rural areas, prison screening services or teenagers,” said Dr Kimmitt,

“The tampon is a small device that can be easily posted to a central laboratory for processing and is less likely to leak than a urine specimen. It is also small enough for easy storage,” the researchers added.

The findings were presented to the Society for General Microbiology meeting in Harrogate. (ANI)

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Light-activated antibacterial coating may help fight hospital-acquired infections

April 1, 2009 By admin Leave a Comment

Washington, Mar 31 (ANI): Scientists at the UCL Eastman Dental Institute have developed a new tool to combat hospital-acquired infections- antibacterial coating that is activated by light.

The research team, led by Zoie Aiken, have tested the new coating with antibacterial properties, and found that it could kill 99.9 percent of Escherichia coli bacteria when a white hospital light was shone on its surface to activate it.

Made of titanium dioxide with added nitrogen, the veneer-like surface, when activated by white light-similar to those used in hospital wards and operating theatres-produced a decrease in the number of bacteria surviving on the test surface.

The hospital environment is usually full of microbes responsible for healthcare-associated infections (HCAI).

Thus, there’s a need for new ways to prevent the spread of these pathogens to patients.

And it is possible to apply antibacterial coatings to frequently touched hospital surfaces to kill any bacteria present and help reduce the number of HCAI.

Titanium dioxide based coatings can kill bacteria after activation with UV light.

And the addition of nitrogen to these coatings enables photons available in visible light to be utilised to activate the surface and kill bacteria.

Aiken said: “The activity of the coating will be assessed against a range of different bacteria such as MRSA and other organisms which are known to cause infections in hospitals. At present we only know that the coating is active against Escherichia coli. However, E. coli is more difficult to kill than bacteria from the Staphylococcus group which includes MRSA, so the results to date are encouraging.

“The coating has currently been applied onto glass using a method called APCVD (atmospheric pressure chemical vapour deposition.

“We are also experimenting with different materials such as plastic. As an example, the coating could be applied to a plastic sheet that could be used to cover a computer keyboard on a hospital ward. The lights in the ward will keep the coating activated, which will in turn continue to kill any bacteria that may be transferred onto the keyboard from the hands of healthcare workers.”

The study was presented at the Society for General Microbiology meeting in Harrogate. (ANI)

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Gene silencing blocks malaria parasites development in multiple mosquito species

March 14, 2009 By admin Leave a Comment

Washington, March 14 (ANI): Researchers at the Johns Hopkins Bloomberg School of Public Health have revealed that they have been able to block the development of the malaria-causing parasite in Anopheles gambiae, A. stephensi and A. albimanus mosquitoes-three mosquito species that spread malaria in Africa, Asia and the Americas-by silencing a gene called caspar.

The researchers revealed that caspar silencing activates the transcription factor Rel 2, a key molecule involved in regulating several potent anti-Plasmodium defence genes that attack the parasite in the mosquito gut.

They said that caspar silencing through the manipulation of gene expression resulted in mosquitoes that successfully blocked the development of Plasmodium falciparum in the gut tissue.

The team said that silencing a gene called cactus, which is part of another pathway called Toll, was also found to have similar effect in controlling the development of Plasmodium berghei, which causes malaria in rodents.

“When a mosquito is feeding on malaria-infected blood, the parasite will be recognized by the mosquito’s immune system through receptors that then start the immune response. In the wild, this response is believed to occur too late to mount an efficient immune defense that would kill all parasites.

At least a few Plasmodia will successfully develop inside the mosquito and enable transmission of malaria,” said Dr. George Dimopoulos, senior author of the study and associate professor at the Johns Hopkins Malaria Research Institute.

“In the lab we activated this immune response in advance of infection, giving the mosquito a head start in defeating the invading parasite,” he added.

The researchers also found that Rel 2 activation did not affect the survival and egg laying fitness of the modified mosquitoes.

“This came as a pleasant surprise since it essentially means that we one day could spread this trait in natural mosquito populations using genetic modification. Furthermore, by activating Rel 2, the genetically modified mosquitoes will attack the malaria parasite with several independent immune factors, and this will make it very difficult for Plasmodium to develop resistance,” said Dimopoulos.

An article on this study has been published in PLoS Pathogens.(ANI)

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Why do people get sick when they’re stressed

March 10, 2009 By admin Leave a Comment

Washington, Mar 10 (ANI): Ever wondered why people get sick when they’re stressed? Well, researchers at UT Southwestern Medical Centre claim to have found the answer.

While studying the diarrhea-causing strain of E coli, they identified a receptor known as QseE, which resides in the bacterium.

The receptor senses stress cues from the bacterium’s host and helps the pathogen make the host ill.

Dr. Vanessa Sperandio, associate professor of microbiology at UT Southwestern and the study’s senior author, said QseE is an important player in disease development because the stress cues it senses from a host, chiefly epinephrine and phosphate are generally associated with blood poisoning, or sepsis.

“Patients with high levels of phosphate in the intestine have a much higher probability of developing sepsis due to systemic infection by intestinal bacteria,” said Dr. Sperandio.

“If we can find out how bacteria sense these cues, then we can try to interfere in the process and prevent infection.

“There’s obviously a lot of chemical signalling between host and bacteria going on, and we have very little information about which bacteria receptors recognize the host and vice versa.

“We’re scratching at the tip of the iceberg on our knowledge of this,” she added.

According to the researchers, once QseC recognizes the stress hormones, it initiates a cascade of genetic activations in which the bacteria colonizes the intestine and moves toxins into human cells, altering the makeup of the cells and robbing the body of nutrients.

“The bacteria get what they want – nourishment – and the person ends up getting diarrhea,” Sperandio said.

“The problem may not only be that the stress signals are weakening your immune system, but that you’re also priming some pathogens at the same time,” she said.

“Then it’s a double-edged sword. You have a weakened immune system and pathogens exploiting it,” she added. (ANI)

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New technique to make bacteria glow under light may help fight against breast cancer

March 8, 2009 By admin Leave a Comment

Washington, March 8 (ANI): Michigan Technological University scientists have come up with a way to make a strain of E. coli glow under fluorescent light, a technique that may one day help track down all sorts of pathogens, and even prove beneficial in fight against breast cancer.

Associate Professor of Chemistry Haiying Liu, who led the research project, points out that E. coli bacteria are naturally found in animal intestines and are usually harmless, but when virulent strains contaminate food, they can cause serious illness and even death.

Liu’s trick takes advantage of E. coli’s affinity for the sugar mannose.

During the study, the research team attached mannose molecules to specially engineered fluorescent polymers, and stirred them into a container of water swimming with E. coli.

The researchers said that microscopic hairs on the bacteria, called pili, hooked onto the mannose molecules like Velcro, effectively coating the bacteria with the polymers.

They later shined white light onto E. coli colonies growing in the solution, and the bugs lit up like blue fireflies.

“They became very colorful and easy to see under a microscope,” said Liu.

The researcher says that this approach may help identify a wide array of pathogens by mixing and matching from a library of different sugars and polymers, which fluoresce different colours under different frequencies of light.

If blue means E. coli, they add, fuchsia may one day mean influenza.

Liu is adapting the technique to combat breast cancer also. In place of mannose, he plans to link the fluorescent polymers to a peptide that homes in on cancer cells.

He says that upon introduction to the vascular system, the polymers would travel through the body, stick to tumour cells, and then illuminated by a type of infrared light that shines through human tissue.

The researcher says that the glowing polymers would provide a beacon to pinpoint the location of the malignant cells, and allow surgeons to easily identify and remove malignant cells while minimizing damage to healthy tissue.

An article on the team’s work on E. coli has been published in the journal Chemistry. (ANI)

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Influenza outbreaks linked to low “absolute” humidity levels

February 10, 2009 By admin Leave a Comment

Washington, Feb 10 (ANI): Ever wondered why we catch flu mostly in the winters? Well, Oregon researchers claim to have found the answer.

They have found that influenza virus survives and travels best when “absolute” humidity is low.

According to lead author Jeffrey Shaman, an Oregon State University, It has long been suspected that there is a link between humidity and flu transmission and prevalence; however, these efforts have focused on relative humidity.

During the study the researchers analysed data from a 2007 study published in PLoS Pathogens, which found a tenuous relationship between influenza transmission and relative humidity.

Shaman used the team’s research data and substituted absolute humidity for relative humidity in analysing potential correlations with flu transmission.

“The correlations were surprisingly strong,” Shaman said.

“When absolute humidity is low, influenza virus survival is prolonged and transmission rates go up,” he added.

The researchers showed that relative humidity only explains about 36 percent of influenza virus survival.

The Oregon researchers retested the data using absolute humidity and found a dramatic rise in accounting for both transmission (50 percent, up from 12 percent) and survival (90 percent, up from 36 percent).

The transmission rates increased from 12 pct to 50 pct while the survival increased to 90 percent from 36 percent.

The potential explanations for influenza peaks during the winter in temperate regions are that people spend more time indoors and thus transmit the virus more easily;

Moreover, less sunlight may have a chemical effect on the virus and/or people’s immune response or there might be an unknown environmental control.

“In some areas of the country, a typical summer day can have four times as much water vapour as a typical winter day – a difference that exists both indoors and outdoors,” Shaman said.

“Consequently, outbreaks of influenza typically occur in winter when low absolute humidity conditions strongly favour influenza survival and transmission,” he added.

The results are published in the Proceedings of the National Academy of Sciences (PNAS).(ANI)

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